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https://hdl.handle.net/2440/9109
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dc.contributor.author | Hogg, A. | - |
dc.contributor.author | Schirm, S. | - |
dc.contributor.author | Nakagoshi, H. | - |
dc.contributor.author | Bartley, P. | - |
dc.contributor.author | Ishii, S. | - |
dc.contributor.author | Bishop, J. | - |
dc.contributor.author | Gonda, T. | - |
dc.date.issued | 1997 | - |
dc.identifier.citation | Oncogene, 1997; 15(24):2885-2898 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.issn | 1476-5594 | - |
dc.identifier.uri | http://hdl.handle.net/2440/9109 | - |
dc.description.abstract | Primary murine fetal hemopoietic cells were transformed with a fusion protein consisting of the ligand-binding domain of the estrogen receptor and a carboxyl-terminally truncated c-Myb protein (ERMYB). The ERMYB-transformed hemopoietic cells exhibit an immature myeloid phenotype when grown in the presence of beta-estradiol. Upon removal of beta-estradiol, the ERMYB cells display increased adherence, decreased clonogenicity and differentiate to cells exhibiting granulocyte or macrophage morphology. The expression of the c-myc, c-kit, cdc2 and bcl-2 genes, which are putatively regulated by Myb, was investigated in ERMYB cells grown in the presence or absence of beta-estradiol. Neither c-myc nor cdc2 expression was down-regulated after removal of beta-estradiol demonstrating that differentiation is not a consequence of decreased transactivation of these genes by ERMYB. While bcl-2 expression was reduced by 50% in ERMYB cells grown in the absence of beta-estradiol, there was no increase in DNA laddering, suggesting that Myb was not protecting ERMYB cells from apoptosis. In contrast, a substantial (200-fold) decrease in c-kit mRNA level was observed following differentiation of ERMYB cells, and c-kit mRNA could be partially re-induced by the re-addition of beta-estradiol. Furthermore, a reporter construct containing the c-kit promoter was activated when cotransfected with a Myb expression vector, providing further evidence of a role for Myb in the regulation of c-kit. | - |
dc.language.iso | en | - |
dc.publisher | STOCKTON PRESS | - |
dc.source.uri | http://dx.doi.org/10.1038/sj.onc.1201472 | - |
dc.subject | Granulocytes | - |
dc.subject | Hematopoietic Stem Cells | - |
dc.subject | Cell Line, Transformed | - |
dc.subject | Macrophages | - |
dc.subject | Fetus | - |
dc.subject | Animals | - |
dc.subject | Mice, Inbred CBA | - |
dc.subject | Mice | - |
dc.subject | Retroviridae | - |
dc.subject | Estradiol | - |
dc.subject | Proto-Oncogene Proteins c-myb | - |
dc.subject | Trans-Activators | - |
dc.subject | Proto-Oncogene Proteins | - |
dc.subject | Receptors, Estrogen | - |
dc.subject | Recombinant Fusion Proteins | - |
dc.subject | DNA | - |
dc.subject | RNA, Messenger | - |
dc.subject | Cell Division | - |
dc.subject | Apoptosis | - |
dc.subject | Cell Differentiation | - |
dc.subject | Down-Regulation | - |
dc.subject | Genes, cdc | - |
dc.subject | Genes, myc | - |
dc.subject | Genetic Vectors | - |
dc.subject | Proto-Oncogene Proteins c-kit | - |
dc.title | Inactivation of a c-Myb/estrogen receptor fusion protein in transformed primary cells leads to granulocyte/macrophage differentiation and down regulation of c-kit but not c-myc or cdc2. | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1038/sj.onc.1201472 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Gonda, T. [0000-0002-8792-3021] | - |
Appears in Collections: | Aurora harvest Medicine publications |
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